The slow growing, maternally inherited (mi) "mutants" of Neuropsora have been investigated in many laboratories over the past twenty years. The altered cytochrome spectra observed in these "mutants" together with the observation that Neurospora mitochondria contain DNA has resulted in research efforts being concentrated on relating the maternally inherited defects to alterations in the mitochondria. These efforts to date have not clearly established the nature of "mitochondrial mutations". Over the past five to ten years it has become clear that filamentous fungi can be infected with viruses, one symptom of such infections being slow growth. Since the "mitochondrial model" does not satisfactorily explain the mi mutants in Neurospora, we screened extracts of certain mi mutants ("poky" and "abnormal") for virus-like particles. Although virus-like particles were not found in our wild type strain, we were able to detect such particles in the mi mutants by electron microscopy. We offer the hypothesis that the mi phenotypes may be manifestations of a viral infection rather than "mitochondrial defects". We propose to establish that there exists a causal relationship between slow growth and the presence of virus-like particles through infectivity studies. We propose to purify these virus-like particles and characterized them as to nucleic acid content and interferon inducing capabilities. The development of these virus-like entities will be studied by sectioning Neurospora protoplasts obtained from glusulase treated mycelium of slow-growing strains. Our electron micrographs suggest that the virus-like particles present in the slow growing strains of Neurospora bear little resemblance to the small polyhedral viruses found in the Aspergilli and Penicillia. This research will begin the characterization of viruses which have previously gone unrecognized. The program proposed will extablish methods whereby the pathogenicity of viruses can be studied in a genetically well defined eucaryotic system.